PMID- 32027625
OWN - NLM
STAT- MEDLINE
DCOM- 20201124
LR  - 20201124
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 26
DP  - 2020 Feb 6
TI  - Knockdown of Long Noncoding RNA (lncRNA) AK094457 Relieved Angiotensin II Induced 
      Vascular Endothelial Cell Injury.
PG  - e919854
LID - 10.12659/MSM.919854 [doi]
AB  - BACKGROUND Hypertension could induce many serious diseases, including damage to 
      vascular endothelial cells. As a non-coding RNA, long noncoding RNA (lncRNA) has 
      received much attention in scientific research and has a regulating efficacy on 
      many critical life activities in human body. The level of lncRNA AK094457 is 
      thought to be elevated in hypertensive rats. However, there is no research 
      indicating the relationship between the level of lncRNA AK094457 and vascular 
      endothelial injury. MATERIAL AND METHODS In our study, we used lentiviral to 
      knockdown lncRNA AK094457, and the human umbilical vein endothelial cells 
      (HUVECs) were stimulated by the Ang II to imitate the vascular endothelial cell 
      damage caused by hypertension. The Cell Counting Kit-8 assays were used to detect 
      the cells viability. Western blotting was performed to detect the endothelial 
      nitric oxide synthase (eNOS), p-eNOS and endothelin-1 (ET-1). After that the 
      production of the NO was monitored. At last, the reactive oxygen species (ROS) 
      levels and apoptosis rates were detected in this study. RESULTS According to the 
      results, we found that knockdown lncRNA AK094457 could alleviate the decrease of 
      vascular endothelial cell viability induced by angiotensin II (Ang II). The 
      knockdown of lncRNA AK094457 also relieved the downregulation of eNOS and p-eNOS, 
      and the decreasing of NO release. At the same time, the knockdown of lncRNA 
      inhibited the levels of Ang II-induced proinflammatory cytokines (tumor necrosis 
      factor [TNF]-alpha, interleukin [IL]-1, and IL-6) and cell adhesion molecules 
      (vascular cell adhesion molecule 1 [VCAM-1], intercellular adhesion molecule 1 
      [ICAM-1], and monocyte chemoattractant protein-1 [MCP-1]). The levels of ROS and 
      apoptosis rates also decreased after the knockdown of lncRNA AK094457. 
      CONCLUSIONS All these results indicated that lncRNA AK094457 could promote Ang 
      II-induced vascular endothelial cell injury. On the contrary, knockdown of lncRNA 
      AK094457 could alleviate this damage.
FAU - Xu, JiaYi
AU  - Xu J
AD  - Department of Gerontology, Minhang Hospital, Fudan University, Shanghai, China 
      (mainland).
FAU - Sun, Yingjie
AU  - Sun Y
AD  - Department of Critical Care Medicine, Minhang Hospital, Fudan University, 
      Shanghai, China (mainland).
FAU - Lu, Jie
AU  - Lu J
AD  - Department of Gerontology, Minhang Hospital, Fudan University, Shanghai, China 
      (mainland).
LA  - eng
PT  - Journal Article
DEP - 20200206
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Inflammation Mediators)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Reactive Oxygen Species)
RN  - 11128-99-7 (Angiotensin II)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.6.3.- (NADPH Oxidase 2)
RN  - EC 2.7.4.3 (Adenylate Kinase)
SB  - IM
MH  - Adenylate Kinase/metabolism
MH  - Angiotensin II
MH  - Apoptosis
MH  - Cell Adhesion Molecules/metabolism
MH  - Cell Survival
MH  - Endothelium, Vascular/*injuries/*metabolism/pathology
MH  - *Gene Knockdown Techniques
MH  - Human Umbilical Vein Endothelial Cells/metabolism/pathology
MH  - Humans
MH  - Inflammation Mediators/metabolism
MH  - NADPH Oxidase 2/metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type III/metabolism
MH  - Phosphorylation
MH  - RNA, Long Noncoding/*genetics/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Up-Regulation
PMC - PMC7020760
COIS- Conflicts of interest None.
EDAT- 2020/02/07 06:00
MHDA- 2020/11/25 06:00
PMCR- 2020/02/06
CRDT- 2020/02/07 06:00
PHST- 2020/02/07 06:00 [entrez]
PHST- 2020/02/07 06:00 [pubmed]
PHST- 2020/11/25 06:00 [medline]
PHST- 2020/02/06 00:00 [pmc-release]
AID - 919854 [pii]
AID - 10.12659/MSM.919854 [doi]
PST - epublish
SO  - Med Sci Monit. 2020 Feb 6;26:e919854. doi: 10.12659/MSM.919854.